EFFECTS OF HEAT ON CELL CALCIUM AND INOSITOL LIPID-METABOLISM
EFFECTS OF HEAT ON CELL CALCIUM AND INOSITOL LIPID-METABOLISM
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DOI：
10.2307/3577239
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发表时间：
1988-03-01
影响因子：
3.4
通讯作者：
HAHN, GM
中科院分区：
文献类型：
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作者：
CALDERWOOD, SK;STEVENSON, MA;HAHN, GM
热疗导致HA-1成纤维细胞内游离钙（[Ca2+]i）大量增加（3 - 5倍）。增加的[Ca2+]i最初似乎是由于Ca2+从内部存储的释放，可能位于内质网。随后观察到细胞外介质中Ca2+的内流。这些热诱导的Ca2+稳态变化与磷酸肌苷（PI）的转换有关，PI是一类磷脂，其代谢已被证明可以调节多种细胞中的Ca2+ （M. J. Berridge和R. F. Irvine, Nature 312, 315(1984)）。45度高温诱导肌醇1,4,5，-三磷酸（IP3）在1分钟内快速释放。C;IP3的释放先于热诱导的[Ca2+]i的升高。IP3的释放是磷脂酶C水解磷脂酰肌醇4,5-二磷酸的结果，是PI转换的第一步。磷脂酸（PI通路中的另一种代谢物）的后期积累与细胞外环境中45Ca2+的延迟、热诱导的内流相关。因此，这些数据表明，热诱导的Ca2+稳态变化与PI转换的激活有关。他们指出，这类脂质可能与热诱导的细胞Ca2+稳态变化密切相关。细胞Ca2+似乎在细胞对热的反应的某些方面是重要的。
Hyperthermia causes a large (three- to fivefold) increase in intracellular free calcium ([Ca2+]i) in HA-1 fibroblasts. Increased [Ca2+]i appears initially to be due to release of Ca2+ from an internal store, probably located in the endoplasmic reticulum. A subsequent influx of Ca2+ from the extracellular medium is then observed. These heat-induced changes in Ca2+ homeostasis are correlated with turnover of the phosphoinositides (PI), a class of phospholipids whose metabolism has been shown to regulate Ca2+ in a wide variety of cells (M. J. Berridge and R. F. Irvine, Nature 312, 315 (1984)). Hyperthermia induces rapid release of inositol 1, 4, 5,-trisphosphate (IP3) within 1 min at 45.degree. C; IP3 release precedes the heat-induced rise in [Ca2+]i. IP3 release, a result of phosphatidylinositol 4,5-bisphosphate hydrolysis by phospholipase C, is the initial step in PI turnover. Later accumulation of phosphatidic acid, another metabolite in the PI pathway, is correlated with the delayed, heat-induced influx of 45Ca2+ from the extracellular environment. The data thus indicate that heat-induced changes in Ca2+ homeostasis are correlated with activation of PI turnover. They indicate that this class of lipids may be closely involved in heat-induced changes in cellular Ca2+ homeostasis. Cell Ca2+ appears to be important in some aspects of the cellular response to heat.